The objective of the research proposed in this application is to generate basic data relating to the circuitry and neurotransmitters responsible for the inhibition of spinal cord motoneurons during active sleep in the adult cat. The animal model which will be employed to achieve this objective is the acute decerebrate cat in which atonia of the peripheral musculature is induced by the microiontophoretic ejection of carbachol, a cholinergic agonist, into the pontine reticular formation. Sucrose gap recordings of inhibitory postsynaptic population potentials of lumbar motoneurons will be averaged and correlated with the discharge, during atonia, of spinal cord interneurons. In addition, intracellular recordings will be obtained from 1) spinal cord motoneurons, 2) extracellular and intracellular recordings will be obtained from spinal cord interneurons that provide a monosynaptic inhibitory input to spinal cord motoneurons, and 3) intracellular and extracellular recordings will be obtained from medullary neurons that provide an excitatory input to spinal cord inhibitory interneurons. The neurotransmitters modulating the excitability of these cells will be examined by recording from them intracellularly at the same time that neurotransmitter antagonists and agonists are ejected juxtacellularly. The proposed studies will 1) provide a description of the cholinergically activated mechanisms and neurotransmitters that produce atonia of the somatic musculature, and 2) establish new techniques and an experimental paradigm that combine the strategic advantages of the acute preparation with a pharmacologically induced pattern of inhibitory motor control that appears identical to that which occurs spontaneously during active sleep in the intact cat.